Entropically Assisted Carbohydrate Recognition by a Natural Killer Cell-Surface Receptor

ChemBioChem ◽  
2004 ◽  
Vol 5 (11) ◽  
pp. 1571-1575 ◽  
Author(s):  
Chittoor P. Swaminathan ◽  
Neelowfar Wais ◽  
Vinay V. Vyas ◽  
Carlos A. Velikovsky ◽  
Alessandro Moretta ◽  
...  
Keyword(s):  
Natural Killer Cell ◽  
Cell Surface ◽  
Natural Killer ◽  
Killer Cell ◽  
Cell Surface Receptor ◽  
Carbohydrate Recognition ◽  
Surface Receptor

Molecular basis of human natural killer cell recognition of HLA-E (human leucocyte antigen-E) and its relevance to clearance of pathogen-infected and tumour cells

2000 ◽  
Vol 99 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Christopher A. O'CALLAGHAN
Keyword(s):  
Endoplasmic Reticulum ◽  
Natural Killer Cells ◽  
Natural Killer Cell ◽  
Cell Surface ◽  
Natural Killer ◽  
Human Leucocyte Antigen ◽  
Killer Cell ◽  
Tumour Cells ◽  
Leader Peptide ◽  
Killer Cells

HLA-E (human leucocyte antigen-E) is a conserved class I major histocompatibility molecule which has only limited polymorphism. It binds to the leader peptide derived from the polymorphic classical major histocompatibility molecules HLA-A, HLA-B and HLA-C. This peptide binding is highly specific and stabilizes the HLA-E protein, allowing it to migrate to the cell surface. A functioning TAP (transporter associated with antigen processing) molecule is required to transport these peptides into the endoplasmic reticulum, where they can interact with HLA-E. HLA-E then migrates to the cell surface, where it interacts with CD94/NKG2A receptors on natural killer cells. This interaction inhibits natural killer cell-mediated lysis of a cell displaying HLA-E. If the leader peptide is not present in the endoplasmic reticulum, HLA-E is unstable and is degraded before it reaches the cell surface. In damaged cells, such as virally infected or tumour cells, down-regulation of HLA-A, HLA-B and HLA-C production or inhibition of TAP prevents stabilization of HLA-E by the leader peptide. Under these circumstances, HLA-E does not reach the cell surface and the cell is then vulnerable to lysis by natural killer cells. The molecular mechanisms underlying this function of HLA-E have been revealed by crystallographic studies of the structure of HLA-E.

scholarly journals Cytomegalovirus m154 Hinders CD48 Cell-Surface Expression and Promotes Viral Escape from Host Natural Killer Cell Control

2014 ◽  
Vol 10 (3) ◽  
pp. e1004000 ◽  
Author(s):  
Angela Zarama ◽  
Natàlia Pérez-Carmona ◽  
Domènec Farré ◽  
Adriana Tomic ◽  
Eva Maria Borst ◽  
...  
Keyword(s):  
Natural Killer Cell ◽  
Cell Surface ◽  
Natural Killer ◽  
Killer Cell ◽  
Surface Expression ◽  
Viral Escape ◽  
Cell Surface Expression ◽  
Cell Control

scholarly journals Associations of Genes for Killer Cell Immunoglobulin-Like Receptors and Their Human Leukocyte Antigen-A/B/C Ligands with Abdominal Aortic Aneurysm

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3357
Author(s):  
Joanna Dubis ◽  
Wanda Niepiekło-Miniewska ◽  
Natalia Jędruchniewicz ◽  
Maciej Sobczyński ◽  
Wojciech Witkiewicz ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Cell Surface ◽  
Killer Cell ◽  
Human Leukocyte ◽  
Cell Surface Receptor ◽  
Single Polymerase Chain Reaction ◽  
Abdominal Aortic ◽  
Surface Receptor ◽  
Hla Ligands

Abdominal aortic aneurysm (AAA) is an immune-mediated disease with a genetic component. The multifactorial pathophysiology is not clear and there is still no pharmacotherapy to slow the growth of aneurysms. The signal integration of cell-surface KIRs (killer cell immunoglobulin-like receptors) with HLA (ligands, human leukocyte class I antigen molecules) modulates the activity of natural killer immune cells. The genetic diversity of the KIR/HLA system is associated with the risk of immune disorders. This study was a multivariate analysis of the association between genetic variants of KIRs, HLA ligands, clinical data and AAA formation. Genotyping was performed by single polymerase chain reaction with sequence-specific primers using commercial assays. Patients with HLA-A-Bw4 have a larger aneurysm by an average of 4 mm (p = 0.008). We observed a relationship between aneurysm diameter and BMI in patients with AAA and co-existing CAD; its shape was determined by the presence of HLA-A-Bw4. There was also a nearly 10% difference in KIR3DL1 allele frequency between the study and control groups. High expression of the cell surface receptor KIR3DL1 may protect, to some extent, against AAA. The presence of HLA-A-Bw4 may affect the rate of aneurysm growth and represents a potential regional pathogenetic risk of autoimmune injury to the aneurysmal aorta.

scholarly journals Evidence that the KIR2DS5 gene codes for a surface receptor triggering natural killer cell function

2008 ◽  
Vol 38 (8) ◽  
pp. 2284-2289 ◽  
Author(s):  
Mariella Della Chiesa ◽  
Elisa Romeo ◽  
Michela Falco ◽  
Mirna Balsamo ◽  
Raffaella Augugliaro ◽  
...  
Keyword(s):  
Natural Killer Cell ◽  
Natural Killer ◽  
Cell Function ◽  
Killer Cell ◽  
Natural Killer Cell Function ◽  
Surface Receptor

scholarly journals Carbohydrate Recognition by a Natural Killer Cell Receptor, Ly-49C

1995 ◽  
Vol 270 (17) ◽  
pp. 9691-9694 ◽  
Author(s):  
Jack Brennan ◽  
Fumio Takei ◽  
Simon Wong ◽  
Dixie L. Mager
Keyword(s):  
Natural Killer Cell ◽  
Natural Killer ◽  
Killer Cell ◽  
Cell Receptor ◽  
Natural Killer Cell Receptor ◽  
Carbohydrate Recognition
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